Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Decreased urinary output (Vu ml/min) after institution of PEEP is attributed to a variety of mechanisms including decreased cardiac output and renal blood flow (RBF), activation of neurohormonal reflexes, increased catecholamines, plasma renin activity (PRA), and antidiuretic hormone (ADH) release. To evaluate these factors, seven normovolemic patients (36 yr +/- 13 SD), free of preexisting lung, cardiac, or renal disease, requiring continuous mandatory ventilation for neurologic reasons were studied. The authors measured or calculated: total blood volume (TBV) (51Cr); right atrial, pulmonary arterial, pulmonary wedge, and systemic pressures, cardiac index (CI); renal plasma flow (RPF) (iodohippurate sodium 131I [131I PAH] clearance); glomerular filtration rate (GFR) (creatinine clearance), free water clearance (CH2O), osmolal clearance (Cosm), fractional excretion of sodium (FENa+) and potassium (FEK+); and plasma renin activity (PRA) (ng X ml-1 X h-1), plasma ADH (pg/ml; radioimmunoassay), epinephrine (E in pg/ml), and norepinephrine (NE in pg/ml) (double-isotope radioenzymatic assay). Two conditions were studied after 90-min steady state: 1) zero PEEP (ZEEP); and 2) 15 cmH2O PEEP. PEEP caused a significant decrease in CI (-21%; P less than 0.01) and RPF (-19%; P less than 0.05) without significant decrease in GFR. A significant decrease in Vu (-55%; P less than 0.05), FENa+ (-39%; P less than 0.05) and Cosm (-36%; P less than 0.25) occurred without modification in CH2O. Plasma ADH remained in the normal range and did not increase when PEEP was applied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:No involvement of antidiuretic hormone in acute antidiuresis during PEEP ventilation in humans. 354 90

One hundred fourteen patients with ruptured cerebral aneurysms were reviewed in regard to the incidence and etiological factors of preoperative disturbances of water and electrolyte metabolism. Patients with inadequate salt intake, evidence of renal disease, cardiac failure or excessive diuretic therapy were excluded. Twenty-five (21.9%) patients developed water and electrolyte disturbances. Hyponatremia (less than 130 mEq/l) occurred in 18 (15.8%) of 114 patients. The majority of those patients with hyponatremia showed laboratory findings and/or clinical features suggesting the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The mean interval between the last subarachnoid hemorrhage (SAH) and the development of hyponatremia was 13.5 days (range 6 to 26 days). No patients developed hypernatremia (more than 155 mEq/l). Preoperative diabetes insipidus (DI) occurred in 7 (6.1%) of 114 patients. The mean interval between the last SAH and the onset of DI was 26.5 days (range 15 to 35 days). When compared with the onset of hyponatremia following SAH, the development of DI was significantly delayed. The present study showed that the following five types of patients significantly related to the development of preoperative water and electrolyte disturbances after SAH due to cerebral aneurysms. The patients with ruptured aneurysms of anterior communicating, anterior cerebral artery or internal carotid artery. The patients in grade III, IV according to Hunt & Hess. The patients with high density in the basal subarachnoid space on the CT scan. The patients with a small hematoma in the region of the basal frontal interhemispheric fissure in cases with aneurysms of the anterior communicating or anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Etiology of water and electrolyte metabolism imbalance following the rupture of cerebral aneurysms--with special reference to preoperative condition]. 646 63

In this retrospective multicentric study, we report on early deaths (ie, those that occurred during the first month of treatment) in a total of 943 newly diagnosed ALL pediatric patients registered from 1976 to 1981 at 21 centers of the AIL- AIEOP . Objectives of this study were as follows: (1) to verify the incidence and the cause of early death in a wide population of children with ALL and (2) to elucidate factors associated with early death and therefore to identify "high-risk" groups of patients. Out of the 943 ALL patients, 39 (4.1%) early deaths were registered. Main causes were infection, 20 patients (51.3%); hemorrhage, 11 patients (28.3%); uric acid nephropathy, 2 patients (5.1%); cardiac failure, 3 patients (7.6%); syndrome of inappropriate antidiuretic hormone secretion, 1 patient. Two patients died during the first week of unknown cause. Thirteen factors measured at diagnosis and possibly influencing the early death rate were analyzed. Using the chi-square test, only three of these factors (age, mediastinum status, surface markers) appear to have any significant influence on the early death rate. We also tried to determine how therapy influences this process by analyzing variations in the early death rate, other factors being equal. Significant differences in the early death rates were encountered in AIEOP protocols using different induction regimens.
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PMID:Early deaths in acute lymphoblastic leukemia (ALL): results of the Italian Pediatric Cooperative Group for Therapy of Acute Leukemia (AIL-AIEOP). 658 79

Plasma concentration (PAVP) and urinary excretion (UAVP) of arginine-vasopressin were studied in 8 patients with primary aldosteronism (PA) during a 36 hour period of fluid restriction in relation to the disturbances of their maximal renal concentrating capacity. The results in untreated patients suffering from PA were compared with the findings in patients after a successful treatment of PA as well as with the results in 9 control subjects. The reduction of maximal renal concentrating ability in PA before the treatment was accompanied with a high excretion of UAVP and the physiological reaction of PAVP to dehydration. Together with the shift of the regression line of the dependence of UOsm on UAVP to higher values of UAVP this indicates a decrease of the sensitivity of the nephrons to the sufficiently high concentrations of endogenous AVP. The increase of renal AVP clearance in PA participates in the high urinary excretion of AVP. The disturbance of the renal concentrating ability as well as the changes of urinary AVP in PA are mostly reversible. After the successful treatment of PA and the completion of potassium stores in the body as well as the healing of the kaliopenic nephropathy, the maximal renal concentrating capacity and AVP gradually return to values close or equal to those in healthy subjects.
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PMID:Plasma concentration and urinary excretion of arginine-vasopressin in primary aldosteronism during the fluid deprivation tests. 668 50

Because lithium salts are widely used for long-term therapy of affective disorders and have been recently implicated as a cause of tubulointerstitial renal disease, we have undertaken experiments designed to establish the site of the early and late pathologic lesions and to determine their correlation with the lithium-induced concentrating defect. Male Wistar rats given a semisynthetic diet that contained lithium carbonate, 90 mEq/kg dry weight, developed serum lithium levels in the human therapeutic range; pair-fed controls received sodium carbonate. Within 3 weeks, treated rats developed marked polyuria, with elevation of free water clearance and vasopressin-resistant diabetes insipidus. Early morphologic changes were confined to the cortical collecting tubules and, possibly, contiguous portions of distal tubules. The tubules were dilated and irregularly lined with cells that had bulging or thinned basophilic cytoplasm, enlarged nuclei, sometimes basal vacuolization, and a few mitoses. These changes were evident at 3 weeks and progressed through the end of the observation period at 18 weeks. The proliferative component of the lesion was demonstrated by the finding of a significant and specific increase in 3H-thymidine uptake by nuclei of collecting/distal tubules of lithium-treated rats. The lesion, but not the increased thymidine uptake, extended into the medullary collecting ducts at 9 and 18 weeks. Although occasional intratubular mononuclear cells were seen at 9 and 18 weeks, no interstitial inflammation or fibrosis was seen. These tubular epithelial lesions were not seen in the kidneys of Brattleboro rats or glucose-treated Wistar rats despite comparable polyuria. We suggest that this early, persistent, and reproducible lesion, characterized by reactive and proliferating tubular cells in the cortical collecting tubules, predisposes the kidney to injury from otherwise mild or insignificant insults and may explain the sporadic occurrence of serious tubulointerstitial disease in patients on long-term lithium therapy.
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PMID:Effects of long-term lithium administration on renal structure and function in rats. A distinctive tubular lesion. 671 69

A number of advances which took place during the last decade have increased our understanding of the physiology and pathophysiology of urinary concentrating defects. The development of a highly sensitive radioimmunoassay for plasma vasopressin concentration has shed new light on vasopressin control mechanisms. The cellular action of vasopressin in biological membranes has been studied by various techniques. The role of adenylate cyclase, cyclic adenosine monophosphate (cAMP), microtubules, and microfilaments, in the response of vasopressin-sensitive membranes is now partially understood. New models of countercurrent multiplication systems, in which urea plays a prominent role, offer a better explanation of certain experimental facts. Such advances had permitted a better understanding of clinical conditions characterized by concentrating defects, including hyperkalemia, hypercalcemia, parenchymal renal disease, obstructive renal disease, and polyuria induced by certain drugs.
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PMID:Pathophysiology of renal concentrating defects. 679 72

Xanthopterin (XPT), an unconjugated pteridine compound, affects cell growth and differentiation. When injected into rats, XPT has caused changes that have been interpreted as renal growth and hypertrophy. In the present study, we investigated the effect of intraperitoneal administration of XPT on the renal function in the rat. XPT administration was associated with polyuria and a reversible form of nonoliguric acute renal failure (ARF), with renal function declining maximally after 2 days and returning to normal after 7 days. The polyuria was due, at least in part, to a concentrating defect that was vasopressin resistant. The ability of XPT to induce ARF was modulated by dietary salt intake, being enhanced by a low-sodium diet and prevented by a high sodium intake. Histological examination of the kidneys showed intratubular crystal deposition and acute tubule necrosis, suggesting that XPT induces crystal nephropathy. There was an increase in wet and dry weights of the kidney and an increased DNA/protein ratio, compatible with a hyperplastic response. Because the severity of other crystal nephropathies may be modulated by urine flow rate and pH, we studied the ability of water diuresis or alkaline diuresis to protect against XPT-induced ARF. Both water diuresis and HCO3 loading blunted the ability of XPT to decrease renal function. The change in renal function induced by XPT in the various groups was paralleled by corresponding changes in the levels of XPT-like substances in the kidney and by the amount of crystal deposition. Thus, XPT injection induces crystal nephropathy, the severity of which can be modulated by dietary salt intake, urine pH, and urine flow rate.
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PMID:Xanthopterin-induced renal dysfunction: a reversible model of crystal nephropathy. 789 1

1. The relationship between vasopressin and the progression of renal failure has been proposed, but not intensively investigated because of a lack of orally available, selective vasopressin antagonists. 2. The effects of novel, orally available vasopressin V1 and V2 receptor antagonists on several indices of the progression of chronic renal failure, i.e. blood pressure, urinary protein excretion, sodium balance and renal histopathology, were investigated by using Wistar rats with adriamycin-induced nephropathy accelerated by deoxycorticosterone acetate-salt hypertension. Groups 2 and 3 were treated with V1 and V2 antagonists, respectively, while the untreated group 1 served as the control. To block the effects of vasopressin efficaciously, V1 and V2 antagonists were simultaneously administered (group 4). 3. At week 6, 2 weeks after the beginning of administration of deoxycorticosterone acetate-salt and vasopressin antagonists after the second injection of adriamycin, V1 and V2 antagonists given either alone or in combination significantly reduced the systolic blood pressure as compared with the control, and urine volume was increased in groups 3 and 4. The proteinuria was also decreased at week 10 in groups 2, 3 and 4. Differences in sodium excretion between all groups were not significant. Histopathological alterations in the kidneys of group 4 were significantly ameliorated. 4. These results suggest that a combination of V1 and V2 antagonists can have therapeutic effects in certain types of chronic renal failure.
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PMID:Effects of vasopressin V1 and V2 receptor antagonists on progressive renal failure in rats. 816 33

The relationship between erythrocyte sodium lithium countertransport activity (SLC), total exchangeable sodium (NaE), and hormonal control of renal function was examined in 40 normotensive, normoalbuminuric, non-neuropathic Type 1 diabetic subjects, of whom 8 had elevated SLC (> 0.40 mmol Li h-1l-1 rbc). Eleven health controls with normal SLC, who were of comparable age, body mass, and blood pressure were also studied. By contrast with healthy controls, SLC in Type 1 diabetes was not associated with plasma renin activity (PRA), aldosterone, systolic blood pressure or lean body mass. SLC was also unrelated to atrial natriuretic peptide (ANP) (Type 1 diabetes only) and NaE. NaE was not correlated with any other variables. The relationships between PRA and aldosterone in healthy controls were retained in Type 1 diabetes (R2 0.37 supine, p = 0.00001, and 0.27 ambulant, p = 0.0005), as were respective direct and inverse relations between vasopressin and ANP and both PRA (rs 0.54 to 0.57, rs -0.43 to -0.53), and aldosterone (rs 0.78 to 0.80, rs -0.71 to -0.80). Fasting free serum insulin and vasopressin were both inversely related to ANP (rs -0.91 and -0.71, respectively). In the absence of autonomic dysfunction, hypertension or early nephropathy in Type 1 diabetes, increased SLC or exchangeable sodium were unrelated to each other or with hormonal control of sodium balance, but the homeostatic factors controlling hormonal interaction appear to be maintained. The interaction between insulin and hormonal control of sodium and water balance may be modified by circulating free insulin concentrations.
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PMID:Increased red cell sodium lithium countertransport activity, total exchangeable sodium, and hormonal control of sodium balance in normoalbuminuric type 1 diabetes. 828 27

We explored the role of angiotensin II and vasopressin in the maintenance of blood pressure during the nephrotic syndrome of adriamycin-induced nephropathy in rats. All 91 rats treated with adriamycin developed chronic renal failure with nephrotic syndrome, which was more pronounced in the normotensive rats than the 35% who became hypertensive. Angiotensin II blockade with DuP 753 produced a significantly greater hypotensive response in both the adriamycin-hypertensive (-16 +/- 3 mm Hg) and adriamycin-normotensive (-14 +/- 5 mm Hg) groups than the saline-treated controls (-5 +/- 1 mm Hg, P < .05). Vasopressin blockade with either a V1V2 inhibitor or a selective V1 inhibitor produced a hypotensive response in adriamycin-hypertensive rats only (by -16 +/- 4 and -17 +/- 2 mm Hg, respectively, P < .01), although the nonselective vasopressin inhibitor produced similar fluid loss and body weight reduction in all three groups. The data suggest that in adriamycin-induced nephropathy with nephrotic syndrome, angiotensin II contributes to blood pressure maintenance in both hypertensive and normotensive animals, whereas the pressor action of vasopressin contributes to elevated blood pressure in hypertensive animals only.
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PMID:Pressor mechanisms in adriamycin-induced nephropathy with hypertension in rats. 828 68


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